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202 > Parkinson’s Disease And Drug Therapy > Flashcards

Parkinson’s Disease And Drug Therapy Flashcards

1
Q

Disturbance of planning?

A

Apraxia

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2
Q

Ballismus?

A

High amplitude flailing of the limbs on one side of the body

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3
Q

Hemiballismus pathophysiology?

A

Disruption of indirect pathway at STN

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4
Q

What causes hemiballismus?

A

Stroke

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5
Q

Tic disorder?

A

Brief repetitive stereotype movements with a premonitory urge (uncomfortable feeling)

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6
Q

Coprolalia?

A

Swearing

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7
Q

Chorea?

A

Jerky, brief, not repetitive, flowing contracting

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8
Q

Chorea pathophysiology?

A

problem in STN in indirect pathway

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9
Q

What causes chorea?

A

Huntington’s and neuroleptics

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10
Q

Huntington’s chorea genetics?

A

Trinucleotide repeat chromosome 4

Autosomal dominant

Longer the repeat sequence the earlier the disease presents

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11
Q

Myoclonus?

A

Brief movement, rapid onset and offset. Positive and negative

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12
Q

Causes of myoclonus

A

Prion
Juvenile myoclonus epilepsy
Brain hypoxia

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13
Q

Dystonia?

A

Abnormal twisting posture, may be associated with jerking movement

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14
Q

Possible pathophysiology for dystonia?

A

Abnormal dopaminergic activity in basal ganglia: blocking dopamine receptors and treatment with levodopa

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15
Q

Dystonia causes?

A

Huntington’s, Parkinson’s, encephalitis, stroke, brain injury

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16
Q

Kinetic tremor?

A

Nose finger

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17
Q

Essential tremors

A

Predominantly postural

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18
Q

Essential tremor is due to?

A

Gabaergic dysfunction in cerebellum

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19
Q

Problems with dopamine blocking agents?

A

Oculogyric crisis (spasmodic movements of eye usually upwards), neuroleptic malignant syndrome

Subacute: drug induced Parkinsonism

Long term: tardive dyskinesia

20
Q

Parkinsonism triad of symptoms?

A

Bradykinesia, rigidity and shaking (resting tremor)

21
Q

Parkinson’s: REM parasomnia?

A

Sleep disorders, unusual movement, emotion, behaviour and dreams between different stages of sleep

22
Q

Pathophysiology of PD?

A

Lack of dopamine from substantia nigra

23
Q

Percentage cell loss of dopaminergic cells of substantia nigra?

A

70%

24
Q

Causes of Parkinsonism?

A

Idiopathic over 80, diffuse levy body, drugs, hydrocephalus, Wilson’s disease, rare familial, cerebri vascular disease

25
Q

Break-down of levodopa?

A

Dopa decarboxylase

26
Q

MAO inhibitors: type A and B:

A

A: serotonin, adrenaline, noradrenaline and dopamine

B: dopamine

We use B because selective e.g selegiline and rasagiline

27
Q

COMT inhibitor?

A

Entacapone/tolcapone.

Makes dyskinesia worse, diarrhoea, liver disease

28
Q

Dopamine agonists?

A

Work on dopamine receptors

Cons, Dopamine dysregulation syndrome

E.g apomorphine s/c infusion but skin nodules

29
Q

Disturbance of coordination is called?

A

Ataxia

30
Q

Example of tic disorders?

A

Simple- coughing blinking
Complex- twirling jumping
Plus motor disorder and coprolalia

31
Q

How do you reduce tic disorder?

A

Distraction and concentration

32
Q

What is the more sever expression of spectrum of tic disorders?

A

Tourette syndrome

33
Q

Tic disorder causes?

A 
Complex genetic inheritance
Post infectious immune
Often associate with other co-morbid conditions 
50%- ADHD
33.3% - OCD
And up to 50% with anxiety
34
Q

What is the clinical presentation of Huntington’s?

A

Cognitive- inability to make decisions multitask and slowness of thought

Behavioural- irritability, depression apathy anxiety delusions

Physical- chorea, motor persistence dystonia and eye movements

35
Q

What can myoclonus be treated by?

A

Antiepilieptics

36
Q

What is th pathophysiology of tremor?

A

Increased activity in the cerebellothalamocortical circuit

37
Q

PD is due to?

A

Dopamine dysfunction in the pallidus

38
Q

Drugs to treat hyperkinetic movement disorders?

A

Dopamine receptor blocking agents
(eg haloperidol, chlorpromazine, pimozide, risperidone)

Dopamine depleting agents
(eg Tetrabenazine, Reserpine)

Atypical anti-psychotics
(eg Clozapine, Olanzapine, Aripiprazole)

39
Q

Oculogyric crisis?

A 
Very characteristic acute response to certain drugs
Fixed stare, upward deviation of eyes
Neck extension
Trunk extension
Jaw spasms +/- tongue protrusion
‘Acute dystonic’ reaction
40
Q

Neuroleptic malignant syndrome?

A

Rigidity/ muscle breakdown – raised CPK.
●Fever
●Autonomic instability (volatile BP/PR)
●Confusion

41
Q

Tardive dyskinesia?

A

Choreic oral-facial movements (video), dystonic trunk posturing
●Exact mechanism unclear – likely dopamine supersensitvity of basal ganglia –ie secondary receptor/ plastic changes
●Treatment -gradual withdrawal of offending agent, substitution with an atypical anti-psychotic ; use of a dopamine depleting agent (tetrabenazine); use of a benzodiazepine (clonazepam) if distressing

42
Q

No motor symptoms of Parkinson’s?

A 
Depression anxiety
Dementia: slowed thoughts
Postural hypotension, hypersalivation
Restless legs rem parasomnia
Reduced sense of smell
43
Q

PD pathophysiology?

A

Decreased dopamine input leads to reduced activation of direct pathway and reduced inhibition of indirect pathway, leading to reduced movements

44
Q

What else do you find in Parkinson’s?

A

Lewy bodies and intraneuronal protein inclusion

45
Q

Early drug therapies for Parkinson’s?

A

Amantadine – Initially anti-flu agent
Glutamate agonist

Anti-cholinergics – Procyclidine, Benzhexol
May help with tremor
Limited by side effects
(confusion, urinary retention, dry mouth…)

Mono-amine oxidase inhibitors

46
Q

Non drug therapies?

A

Not clear how it works (but it does!)
Probably high freq stimulation
causing ‘jamming’(inhibition of
neurons by depolarising block)

Also disrupts abnormally
synchronous basal ganglia rhythms

Favoured target
subthalamic nucleus (STN) for PD
Also pallidum (for dystonia)
and thalamus (for tremor)
Disease will still progress
and no effect on non-motor
-dementia,
-dysautonomia,
-postural instability…..
  • Future – neurorestorative (stem cells)
  • Neuroprotective (growth factors)

202 (58 decks)

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